The prevalence of allergic diseases has constantly increased in the developed countries during recent decades. The immune system of a newborn infant is immature, and develops during the first months and years of childhood. Healthy children develop an immune response against pathogens in their environment, whereas an increasing proportion of the children develop an allergic response against non-harmful factors in the environment leading to allergic diseases.
Several attempts have been made to prevent the development of allergic diseases. For many years exclusive breast-feeding, and avoidance of contact with possible allergenic sources such as cats and dogs in early childhood have been implicated as means for decreasing the risk of allergic diseases. However, the results have not been convincing.
A more recent hypothesis for the cause of allergic diseases is the “hygiene hypothesis”, which is based on the fact that the prevalence of allergic diseases is significantly higher in prosperous countries with high standards of living and hygiene, than in countries having lower standards of hygiene. Further an inverse association between the number of siblings and allergic diseases has been documented in epidemiological surveys [1,2]. Growing up on a farm seems to be associated with a lower prevalence of allergic rhinitis and sensitization [3, 4, 5]. Children who do not live on a farm but have regular contact with livestock had also a lower prevalence of allergic sensitization [4]. The underlying reasons behind these associations are largely unknown, but the “hygiene hypothesis” provides a possible explanation suggesting that exposure to a variety of microbes in childhood protects against allergic diseases by promoting the maturation of the immune system [2,6]. One possible approach to tackle allergy has been the administration of probiotic bacteria, especially lactic acid bacteria, which have been shown to promote a tolerogenic immune response.
Several studies have suggested a role for Th2-polarized CD4+ T cells in the pathogenesis of asthma and allergy [7-9] but the exact immunological mechanisms regulating allergic sensitization are not known. Th1-biased immune responses may down-regulate the effects of Th2 cells [7] or regulatory T cells may control the function of both Th1 and Th2 cells as well as the Th1/Th2 balance [8, 9]. Although some reports are contradictory, there is epidemiological support that some infections, such as hepatitis A virus (HAV) [10-13], Toxoplasma gondii [12, 13] and Helicobacter pylori [12-14] and bacterial components [15-17] are associated with a reduced risk of allergic diseases, thus supporting the hypothesis that the microbial load is an important environmental factor conferring protection against the development of allergies in childhood [18]. Moreover, an independent inverse association was observed between the number of gastrointestinal infections before the age of 5 years and the risk of atopy in the UK [19]. It has also been reported that early childhood infection with human herpes virus type 6 (HHV-6) could protect against the development of IgE sensitization, atopic disease and allergy in young children (WO2006/031195).
However, not all microbial infections have a protective effect on the prevalence of atopic diseases. It was for example found that seropositivity for intestinal bacterial pathogens such as Clostridium difficile, Campylobacter jejuni and Yersinia enterocolitica was associated with a higher prevalence of atopy among Danish adults [13]. Recently Benn et al. reported that infectious diseases during the first 6 months of life (mostly upper respiratory infections) increase the risk of atopy [20], and Bager and collaborators observed a growing risk of atopy with increasing number of infections caused by airborne viruses (measles, rubella, mumps and varicella) before the age of 1 year [21].
There is a definite need of effective means for decreasing the risk of allergic sensitization and thereby preventing or treating diseases associated therewith. In particular there is a need of preventing the development of allergic diseases such as asthma, eczema, allergic rhinitis and conjunctivitis and food-induced allergies. The present invention meets these needs.